肾纤维化的最新进展和治疗方法:临床证据。

Mansi Sharma, Mansi Khanna, Pranjal Kumar, Ghanshyam Das Gupta, Kalicharan Sharma
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引用次数: 0

摘要

背景:纤维化是一种病理并发症,由组织对慢性炎症或反复损伤的异常愈合反应引起。其特点是细胞外基质(ECM)过度沉积,导致进行性器官功能障碍。病因不明的慢性肾脏疾病(CKDu)是一种新认识的公共卫生危机,其特点是缓慢,不可逆的进展和晚期无症状发作。目的:确定和分析肾纤维化的治疗靶点、实验策略和新兴治疗方法,重点是CKDu。方法:对CCR1抑制剂、CCL2- CCR2抑制剂、CTGF抑制剂、ET-1拮抗剂、Nox1/4抑制剂、TGF-β拮抗剂、TNF-α拮抗剂等潜在治疗靶点的实验数据进行整理和分析。我们特别关注Cx43 (Connexin 43)和DDR1 (Discoidin Domain Receptor 1)在纤维化中的作用。收集和回顾了植物药物(如LIVON-S(水飞蓟素)和生物纤维蛋白)以及干细胞疗法等新兴治疗方法的数据。结果:治疗靶点涉及纤维化发生的关键分子通路,包括趋化因子信号(CCR1、CCR2和CCL2)、促纤维化介质(TGF-β和CTGF)和氧化应激(Nox1/4)。植物药物,如水飞蓟素和生物纤维蛋白,通过其抗炎和ecm调节作用显示出抗纤维化潜力。干细胞治疗的临床前研究强调了治疗肾纤维化的再生益处。Cx43和DDR1的实验数据支持它们在纤维化进展中的作用和作为治疗靶点的潜力。结论:该研究提供了抗纤维化策略的全面分析,包括经过验证的分子靶点、植物药物和干细胞治疗等创新疗法。这些发现强调了重点研究和开发CKDu及相关纤维化疾病的有效干预措施的必要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Recent Progression and Treatment Approaches of Kidney Fibrosis: Evidence to Clinic Approach.

Background: Fibrosis is a pathological complication that arises from an abnormal tissue healing response to chronic inflammation or repeated injury. It is characterized by Excessive Extracellular Matrix (ECM) deposition, leading to progressive organ dysfunction. Chronic Kidney Disease of unknown etiology (CKDu) is a newly recognized public health crisis characterized by slow, irreversible progression and late-stage asymptomatic onset.

Objectives: To identify and analyze therapeutic targets, experimental strategies, and emerging treatments for renal fibrosis, with a focus on CKDu.

Methods: Experimental data on potential therapeutic targets, including CCR1 inhibitors, CCL2- CCR2 inhibitors, CTGF inhibitors, ET-1 antagonists, Nox1/4 inhibitors, TGF-β antagonists, and TNF-α antagonists, were compiled and analyzed. Specific attention was given to the roles of Cx43 (Connexin 43) and DDR1 (Discoidin Domain Receptor 1) in fibrosis. Data on phytopharmaceuticals, such as LIVON-S (Silymarin) and bio-fibrin, as well as emerging treatments like stem cell therapies, were gathered and reviewed.

Results: Therapeutic targets address key molecular pathways involved in fibrogenesis, including chemokine signaling (CCR1, CCR2, and CCL2), pro-fibrotic mediators (TGF-β and CTGF), and oxidative stress (Nox1/4). Phytopharmaceuticals, such as silymarin and bio-fibrin, demonstrated antifibrotic potential through their anti-inflammatory and ECM-modulating effects. Preclinical studies on stem cell therapies highlighted regenerative benefits in managing renal fibrosis. Experimental data on Cx43 and DDR1 supported their role in fibrotic progression and potential as therapeutic targets.

Conclusion: The study provides a comprehensive analysis of antifibrotic strategies, including validated molecular targets, phytopharmaceuticals, and innovative therapies like stem cell treatments. These findings underscore the need for focused research and development of effective interventions for CKDu and related fibrotic diseases.

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